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The specific application is a study of the morphological change in a mouse placenta induced by knocking out the retinoblastoma gene.
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The presence of pathogenic organisms in the placenta induces a maternal immune response to infection that could result in miscarriage.
This shortened period of placental maturity relative to the gestational period could render the mouse placenta particularly susceptible to stress induced by defective utilization of nutrients and/or impaired calcium metabolism in the context of mitochondrial dysfunction.
This technique confirms the vast knowledge we have concerning mouse placenta histology and is therefore an excellent tool for studying blood flow within the placenta during infectious pathologies.
In addition, 90 of the 2,963 genes expressed in placentas of human, mouse, and elephant also cause abnormal mouse placenta morphology and/or physiology when knocked out in the mouse.
Our results show that Cacnb3 exhibits specific spatial and temporal expression in the mouse placenta.
To determine the role of CACNB3 in the mouse placenta, we performed an expression and function analysis.
To date, an empirical validation of reference genes suitable for RT-qPCR-based studies in the mouse placenta is missing.
These three genes are imprinted in the mouse placenta.
The transporter genes Slc22a2 and Slc22a3 are imprinted specifically in mouse placenta [32].
Mouse placenta is positive for Peg10 transcripts as well as the Peg10-RF1 Peg10-RF1/2 Peg10-RF1/2s [7].
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